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Vitamin Deficiencies – Diagnosis and Treatment
Published in Jennifer Doley, Mary J. Marian, Adult Malnutrition, 2023
Wernicke-Korsakoff’s syndrome includes Wernicke’s encephalopathy and Korsakoff’s syndrome, which are distinct disorders but often occur together in patients with AUD who do not consume adequate amounts of thiamin-fortified foods. Wernicke’s encephalopathy is characterized by psychomotor slowing, nystagmus, ataxia, ophthalmoplegia (paralysis or weakness of eye muscles), and impaired consciousness. Korsakoff’s syndrome is characterized by memory deficits. If left untreated Wernicke-Korsakoff’s syndrome will lead to coma and death.11
Movement disorders
Published in Ibrahim Natalwala, Ammar Natalwala, E Glucksman, MCQs in Neurology and Neurosurgery for Medical Students, 2022
Ibrahim Natalwala, Ammar Natalwala, E Glucksman
v – The classic triad of ophthalmoplegia (paralysis of one or more eye muscles), ataxia and confusion is highly suggestive of Wernicke’s encephalopathy. The patient is also starting to show signs of progression to Korsakoff’s syndrome, which consists of memory lapses, confusion and confabulation. The ophthalmoplegia should distinguish this diagnosis from that of Parkinson’s disease.2
Introduction to dementia
Published in Joanne Brooke, Dementia in Prison, 2020
Experts recommend that anyone with a history of heavy alcohol consumption who experiences symptoms associated with Wernicke encephalopathy should be given injectable thiamine until the clinical picture is clearer (Martin et al., 2003). Once acute symptoms improve, individuals should be carefully evaluated to determine if their medical history, alcohol use and pattern of memory problems may be consistent with Korsakoff syndrome. For those who develop Korsakoff syndrome, extended treatment with oral thiamine and magnesium as well as a reduction in alcohol intake may increase chances of symptom improvement. If there is no improvement, consideration should be given to treatment of comorbid deficiencies and other medical conditions (Martin et al., 2003).
Peripapillary Retinal Haemorrhages in Wernicke’s Encephalopathy Following Bariatric Surgery in a Young Patient
Published in Neuro-Ophthalmology, 2022
Motazz A. Alarfaj, Nada H. Almadhi, Mohammad Al-Amry, Abdullah I. Almater, Majed Al-Obailan
Vitamin B1, or thiamine, is a water-soluble vitamin that functions as a cofactor for energy production. There is a limited intracellular reserve so constant cellular resupply is needed.1 Thiamine deficiency can manifest with two clinical phenotypes: Wernicke-Korsakoff’s syndrome and beriberi. Wernicke’s encephalopathy is characterised classically by a triad of ophthalmoplegia, confusion, and ataxia. Korsakoff’s syndrome (KS) occurs as a late complication of WE and is defined by memory impairment associated with confabulation. KS has a mortality rate of 20% if left untreated. Beriberi may present with congestive cardiac failure (wet beriberi) or polyneuropathy (dry beriberi).1 WE can occur in the setting of poor nutrition or absorption, for example, after bariatric surgery. Whenever there is clinical suspicion, thiamine replacement should be started immediately because of the cognitive consequences of any delay. Herein, we describe a case of WE following laparoscopic sleeve gastrectomy in a young male patient who presented with binocular horizontal diplopia and was found to have preretinal peripapillary haemorrhages.
Thiamine and phosphate esters concentrations in whole blood and serum of patients with alcohol use disorder: a relation with cognitive deficits
Published in Nutritional Neuroscience, 2021
Laurent Coulbault, Ludivine Ritz, François Vabret, Coralie Lannuzel, Céline Boudehent, Marie Nowoczyn, Hélène Beaunieux, Anne Lise Pitel
However, TD is not systematically found in AUD patients without neurological complication. In a study by Tallaksen et al., differences were observed between controls and AUD patients for thiamine (Th) and thiamine monophosphate (TMP) concentrations in whole blood and serum, but not for TDP [12]. The authors showed also that thiamine was not fully phosphorylated after supplementation. In addition, a recent study did not find any TD in a population of AUD patients with cognitive deficits, probably related to an efficient thiamine supplementation in these patients reflecting good clinical practice [13]. In another study conducted in AUD patients with Korsakoff’s syndrome, thiamine metabolism was dramatically impaired after supplementation, suggesting a link between alterations of thiamine metabolism and the severity of the cognitive deficits [14]. Another study also suggested a potential interest for the exploration of altered thiamine metabolism (using percentage of thiamine phosphate esters in WB) in alcohol-related cognitive deficits and more particularly in episodic memory impairments well before the development of Korsakoff’s syndrome [15].
Errorless (re)learning of everyday activities in patients with Korsakoff’s syndrome: A feasibility study
Published in Neuropsychological Rehabilitation, 2019
Yvonne C. M. Rensen, Jos I. M. Egger, Josette Westhoff, Serge J. W. Walvoort, Roy P. C. Kessels
Chronic and excessive alcohol use can affect the brain, resulting in varying degrees of cognitive impairment. Cognitive deficits in multiple cognitive domains can be found in individuals with alcohol-related brain damage, but often encompass episodic memory (Ihara, Berrios, & London, 2000; Pitel et al., 2007) and executive function (Ihara et al., 2000; Noel et al., 2001). The most severe neuropsychiatric disorder that is commonly associated with alcoholism is Korsakoff’s syndrome. Korsakoff’s syndrome is a neuropsychiatric disorder, typically resulting from thiamine deficiency. A continuity theory has been proposed (Pitel et al., 2008; Ryback, 1971), postulating a progressive increase in brain and cognitive damage between patients with alcohol use disorders with and without Korsakoff’s syndrome (Bowden, 1990; Butters & Brandt, 1985; Parsons, 1998), with Korsakoff’s syndrome covering the most severe end of the continuum. Some recovery of alcohol-related brain damage and cognitive deficits has been observed after weeks, months, or even years of abstinence (Fein, Torres, Price, & DiScalfani, 2006; Pitel et al., 2009; Walvoort, Wester, & Egger, 2013). Approximately 25% of the patients with Korsakoff’s syndrome completely recover, yet in 25% the neurocognitive profile remains unchanged (Kopelman, Thomson, Guerrini, & Marshall, 2009; Victor, Adams, & Collins, 1971).